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- M E O'Dwyer and B J Druker.
- Leukaemia Program, Oregon Health Sciences University, Portland, OR, USA.
- J. Intern. Med. 2001 Jul 1; 250 (1): 3-9.
AbstractThe deregulated tyrosine kinase activity of the BCR-ABL fusion protein is the cause of malignant transformation in almost all cases of chronic myelogenous leukaemia (CML), making BCR-ABL an ideal target for pharmacological inhibition. Signal transduction inhibitor (STI571) (formerly CGP57 148B), is an ABL specific, tyrosine kinase inhibitor. In preclinical studies, it has been shown to selectively kill BCR-ABL expressing cells, both in-vitro and in vivo. The results of clinical studies to date are highly encouraging and STI571 promises to be an important addition to the therapy of CML.
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